title: Hyaluronic acid-dependent protection against UVB-damaged human corneal cells.
abstract: Within ultraviolet radiation, ultraviolet B (UVB) is the most energetic and damaging to humans. At the protein level, UVB irradiation downregulates the expression of antioxidant enzymes leading to the accumulation of reactive oxygen species (ROS). Due to lacking of a global analysis of UVB-modulated corneal proteome, we investigate in vitro the mechanism of UVB-induced corneal damage to determine whether hyaluronic acid (HA) is able to reduce UVB irradiation-induced injury in human corneal epithelial cells. Accordingly, human corneal epithelial cell lines (HCE-2) were irradiated with UVB, followed by incubation with low molecular weight HA (LMW-HA, 100 kDa) or high molecular weight HA (HMW-HA, 1,000 kDa) to investigate the physiologic protection of HMW-HA in UVB-induced corneal injury, and to perform a global proteomic analysis. The data demonstrated that HA treatment protects corneal epithelial cells in the UVB-induced wound model, and that the molecular weight of HA is a crucial factor. Only HMW-HA significantly reduces the UVB-induced cytotoxic effects in corneal cells and increases cell migration and wound-healing ability. In addition, proteomic analysis showed that HMW-HA might modulate cytoskeleton regulation, signal transduction, biosynthesis, redox regulation, and protein folding to stimulate wound healing and to prevent these UVB-damaged cells from cell death. Further studies evidenced membrane-associated progesterone receptor component 1 (mPR) and malate dehydrogenase (MDH2) play essential roles in protecting corneal cells from UVB irradiation. This study reports on UVB-modulated cellular proteins that might play an important role in UVB-induced corneal cell injury and show HMW-HA to be a potential substance for protecting corneal cells from UVB-induced injury.
authors.affiliation: Institute of Bioinformatics and Structural Biology & Department of Medical Sciences, National Tsing Hua University, Hsinchu, Taiwan.
authors.forename: Ji-Min
authors.initials: JM
authors.lastname: Li
authors.forename: Hsiu-Chuan
authors.initials: HC
authors.lastname: Chou
authors.forename: Ssu-Han
authors.initials: SH
authors.lastname: Wang
authors.forename: Chieh-Lin
authors.initials: CL
authors.lastname: Wu
authors.forename: Yi-Wen
authors.initials: YW
authors.lastname: Chen
authors.forename: Szu-Ting
authors.initials: ST
authors.lastname: Lin
authors.forename: Yu-Hua
authors.initials: YH
authors.lastname: Chen
authors.forename: Hong-Lin
authors.initials: HL
authors.lastname: Chan
mesh_terms: D002460:Cell Line; D049109:Cell Proliferation / Q000187:drug effects / Q000528:radiation effects; D002470:Cell Survival / Q000187:drug effects / Q000528:radiation effects; D003315:Cornea / Q000187:drug effects / Q000528:radiation effects; D019610:Cytoprotection; D003599:Cytoskeleton / Q000187:drug effects / Q000528:radiation effects; D004847:Epithelial Cells / Q000187:drug effects / Q000528:radiation effects; D019573:Epithelium, Corneal / Q000166:cytology / Q000187:drug effects / Q000528:radiation effects; D006801:Humans; D006820:Hyaluronic Acid / Q000494:pharmacology*; D008291:Malate Dehydrogenase / Q000235:genetics* / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects / Q000528:radiation effects; D040901:Proteomics; D034622:RNA Interference; D034741:RNA, Small Interfering; D017382:Reactive Oxygen Species / Q000528:radiation effects; D011980:Receptors, Progesterone / Q000235:genetics* / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects / Q000528:radiation effects; D014466:Ultraviolet Rays / Q000009:adverse effects*; D014945:Wound Healing / Q000187:drug effects / Q000528:radiation effects
chemical_list: D034741:RNA, Small Interfering; D017382:Reactive Oxygen Species; D011980:Receptors, Progesterone; D006820:Hyaluronic Acid; D008291:Malate Dehydrogenase
keywords: DIGE; UVB; cornea; hyaluronic acid; proteomics